STARTING 2016 WITH A LAUGH... BY LOOKING ON THE BRIGHT SIDE
In theory, there is no difference between theory and practice. In practice there is.
Listen carefully to first criticisms of your work. Note what it is about your work the critics don’t like—then cultivate it.
That’s the part of your work that’s individual and worth keeping.
Always listen to experts.
They’ll tell you what can’t be done and why.
Then do it.
Speak when you are angry, and you will make the best speech you will ever regret.
THE POLITICOS CAN’T STAND IT WHEN THEY’RE THE BUTT OF LAUGHTER THEY’LL CRINGE AND THEN THEY’LL SLINK AWAY, INTO THE ZOMBIE HEREAFTER.
In the Third Century AD, Emperor Caracalla of the bankrupt Roman Empire was said to have pointed to his sword and remarked “as long as we have this, we shall not run short of money.”
THE WORLD STATE by G. K. Chesterton
Oh, how I love Humanity,
With love so pure and pringlish,
And how I hate the horrid French,
Who never will be English!
The International idea,
The largest and the clearest,
Is welding all the nations now,
Except the one that’s nearest.
This compromise has long been known,
This scheme of partial pardons,
In ethical societies
And small suburban gardens—
The villas and the chapels where
I learned with little labour
The way to love my fellow-man
And hate my next-door neighbor.
The truth will set you free...
But first it will piss you off!
Freedom is the oxygen of the soul.
The Russians are very good at digging mass graves and filling them in, And the Europeans are very good at looking the other way.
* In a report with the headline “Senior Obama officials have warned of challenges in screening refugees from Syria” (The Washington Post, 11/17/15, we get the picture that the risks associated with importing 300,000 Syrian refugees into the United States are severe and there is a substantial problem in imagining what could possibly justify this, e.g., how does the United States benefit from this? What, one has to wonder, is the agenda that the powers that be have in mind?
The Post article (see footnote) quotes FBI director James Cooney as saying in Congressional testimony last month that, although the vetting process for checking out refugees has “‘improved dramatically,’ Syrian refugees will be even harder to check because, unlike in Iraq, U.S. soldiers have not been on the ground collecting information on the local population. ‘If we don’t know much about somebody, there won’t be anything in our data,’ he said, ‘I can’t sit here and offer anybody an absolute assurance that there’s no risk associated with this.’” One might say that he COULD offer an absolute assurance that terrorists will get into the United States via such a plan.
WHEN HISTORY REPEATS— THE COLLAPSE OF THE ROMAN EMPIRE
Rome’s collapse meant staggering loss. People forgot how to read, how to farm, how to govern themselves, how to build houses, how to trade, and even what it had once meant to be a human being.
WHO STEALS THE MOST STUFF IN THE UNITED STATES?
“Law Enforcement took more stuff from people than burglars did last year” proclaimed a headline in the Washington Post 11/23/2015. The Post reports that, as pointed out in the blog from Martin Armstrong of Armstrong Economics the week before and as Armstrong learned from the Institute for Justice, the Treasury and Justice departments deposited more than $5 BILLION into their respective asset forfeiture funds last year, while the FBI reports that burglary losses topped out at $3.5 BILLION. (Needless to say, the total amount of private burglary losses is likely to be underestimated overall but, on the other hand, an unusually large asset seizure can have a very large impact on the total. The article reports that the Bernie Madoff judgment amounted to $1.7 billion, which was said to have reverted largely to the victims (though you have to wonder how much the lawyers got).
Chen et al. Activation of TRPV1 channel by dietary capsaicin improves visceral fat remodeling through connexin43-mediated Ca2+ influx. Cardiovasc Diabetol.14:22 (2015).
The above paper discusses the stimulation by capsaicin (hot pepper) of the burning of fat by adipocytes in visceral fat. Niacin, a TRPV1 agonist, signals brown fat and other types of cells to use fat as a fuel rather than glucose, though we do not have a reference at hand that niacin signals such a switch in fuel use in adipocytes in the heart nor do we know whether capsaicin does that in the heart. This could be important as the heart is highly dependent on fat burning for the production of energy. See Virtue et al. A new role for lipocalin prostaglandin D synthase in the regulation of brown adipose tissue substrate utilization. Diabetes. 61:3139-47 (2012). Prostaglandin D synthase is activated by niacin during the niacin flush. For more, see Sandy Shaw’s niacin flush paper in the August, September, and October Life Enhancement website. Li et al. TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated smooth muscle cells. Cell Death Dis. 5:e1182 (2014).
Foam cells are a major part of the atherosclerotic process. Here, the researchers used smooth muscle cells derived from mice. Capsaicin was used to activate TRPV1.
Suggestion: Take capsaicin capsules as a daily supplement
VITAMIN D3 promotes the recovery of amyloid beta clearance by phagocytes in ALZHEIMER’S DISEASE macrophages derived from human patients.
DAYDREAMS: NOREPINEPHRINE facilitates what is called “task unrelated thoughts” or (more commonly) daydreams.
The data in a paper (Rafi, 2007) indicated potent anti-inflammatory effects of the carotenoid lycopene that, as part of a natural chemical pathway, inhibits COX. Via its two forms COX1 and COX2, COX converts arachidonic acid to inflammatory prostaglandins, such as the powerful inflammatory prostaglandin E2 (PGE2) (though under some conditions PGE2 can be anti-inflammatory). PGE2 is a known factor in virtually all inflammatory diseases, including cardiovascular disease, cancer, diabetes type 2, arthritis, inflammatory bowel disease, epilepsy, Alzheimer’s disease, and many others.
COX-1 is constitutively expressed, while COX-2 is an inducible enzyme that “mediates acute and chronic inflammation, pain, and cellular repair mechanisms.” (Rafi, 2007) The authors believe that the results of data from studies of lycopene “suggest that inhibition of COX2 may be effective in preventing infammatory-associated cancers.” (This suggestion, from 2007, was supported by later work.) The authors concluded: “Therefore, using lycopene or [lycopene-containing] tomato-based products to regulate the production of NO and COX-2 may be classified as a therapeutic approach for the treatment or prevention of chronic inflammatory disease.”
Sandy Gets Some Relief From The Pain Of Her Arthritic Knees With Lycopene
Unfortunately, Sandy has a moderate case of knee osteoarthritis. We had run out of lycopene and after a few days to a couple of weeks she had noticed more pain in her knees. The day she went back on lycopene (we both used 15 mg a day, though Sandy has upped hers to 30 mg a day now that she has felt the difference), she was aware of much more comfort in walking. The best way to take it is with the fattiest meal of the day, as it is absorbed best with fats.
It is also interesting that lycopene is another one of the natural products that inhibits formation of inflammatory prostaglandins. See (Shaw, 2015) “Why the Niacin Flush May Be Surprisingly Beneficial to Your Health” by Sandy Shaw for a discussion in Part I under the subheading “What Is the Niacin Flush? of inflammation and the prostaglandins that play such a major role in it, particularly PGE2 and PGD2. PGD2 is prostaglandin D2 that is released, causing the niacin flush, and which counters the effects of inflammatory PGE2 when released as a pulse, but there are many ways other than taking niacin to interfere with PGE2-induced inflammation. Lycopene is one such effective antiinflammatory nutrient.
Note that COX-2 inhibitors such as Celebrex are widely used for treating arthritis and, unlike the prescription COX-2 inhibiting drugs, there is no evidence that lycopene increases the risk of cardiovascular disease. Indeed, lycopene reduces the risk, possibly (at least in part) because of its powerful antioxidant activity.
Sandy Shaw (2015) paper, Part I, is found in the Life Enhancement website, www.life-enhancement.com, August 2015.
Like any physiological process, there is a level at which too much neurogenesis can lead to adverse effects (Hsieh and Schneider, 2013). The effects of various levels of electrical activity on neurogenesis have been described (Hsieh and Schneider, 2013) as follows: “It may be that the neurogenesis response of stem progenitor cells to [electrical] activity is an adaptive mechanism to maintain regional homeostasis: increasing stem cell production when local circuitry activity levels are low, and restoring quiescence when activity levels are high.” The point here is that when activity levels are too high, you have electrical activation that becomes pathologically high as occurs during an epileptic seizure. As the authors go on to explain: “A potential ‘cost’ of excitable stem cells is inappropriate activation after pathological forms of activity, such as seizures.”
The authors also describe a possible excitation signal as follows: “A possible mechanism for excitation-neurogenesis coupling is GABA-mediated depolarization, previously described in mouse embryonic neuronal progenitor cells. Depolarization causes an increase in intracellular Ca2+ concentration similar to that evoked in cultured neural stem/progenitor cells. This excitation signal is relayed to the genome wherein the transcription factor NeuroD is rapidly activated to promote neurogenesis.” “...excitation signaling in the form of GABA is also necessary to drive the functional integration of newborn neurons.”
In another paper (Veyrac, 2013), the authors explain, “Newborn DGCs [dentate granule cells] are initially tonically activated by ambient depolarizing GABA....” Following hyperpolarization (by process that includes expression of glutamate receptors), “...they are hyperexcitable, display properties of ehanced synaptic plasticity, and are prone to integrate the existing hippocampal neurocircuitry.”
Importantly, the authors point out, “As their functional maturation progresses, however, newborn DGCs compete to survive, leaving the majority eliminated by cell death. Several behavioral manipulations, in particular hippocampal dependent learning, can regulate their rate of survival.” In this paper (Veyrac, 2013), the authors identify the Zif268/egr1 gene as controlling the selection, maturation, and functional integration of adult hippocampal newborn neurons by learning.”
Immediate Early Genes Are Transiently And Preferentially Induced In Newborn DGCs During Their Critical Period Of Maturation
Zif268/egr1 is one such immediate early gene and, as explained in the paper, actively controls the survival of newborn DGCs during their critical period of maturation in the first 2-3 weeks of their birth.”
The requirement for excitation during the early phase of newborn neuronal maturation may be a reason that the decline in arachidonic acid in cell membranes of the brain with aging is a negative factor in cognition (McGahon, 1997). Despite the fact that the metabolic products created by arachidonic acid are often involved in damage due to excessive inflammation, arachidonic acid is there for some reason(s) and this might be one of those reasons. Rice oil is relatively rich in arachidonic acid. Perhaps this is one reason that the Japanese who live in Japan, who consume a lot of rice and use rice oil in cooking, may live longer than those in other countries.
DHA Protects the Brain Against Inflammation
As we have written before, one way to protect the brain against arachidonic acid-associated inflammation is to take supplementary DHA, docosahexaenoic acid, as found in fish oils. (Basselin, 2012).
ORGASM: How the Brain Makes You Feel SOOOOO Good
by Sandy Shaw
HYPOTHESIS: ORGASM is like a small, self-limited epileptic seizure in terms of temporal electrical activity, that takes place in the “pleasure center” area of the brain and also in the lower part of the spinal cord. Feeling good is an important part of what makes life worth living and orgasms make you feel so good.
It is known that people experiencing epileptic seizures may also concurrently have orgasms. An early paper Sandy got after she hypothesized that orgasm might be a sort of small epileptic seizure provides support for that hypothesis (Heath, 1972). It is surprising how some of the oldest papers in a field provide information that has not been referred to in later papers. So, in researching how orgasm works, Sandy decided to look at the early stuff. The Heath, 1972 paper was useful, as was Gil-Vernet, 1994, which provided an amazingly detailed series of events that take place in the ejaculatory mechanisms accompanying orgasm (that include, for example, urethra, prostate, bladder neck, and so on), all via endorectal ultrasonography. Incredible work!
Interestingly, epilepsy has been very recently reported to be associated with activation of the TRPV1 receptor (Naziroglu, 2015), for which capsaicin (component of hot pepper) is an agonist. Anti-epileptic medications which reduce the sensitivity of the TRPV1 receptor to its agonists, tend to increase the difficulty of reaching orgasm. The TRPV1 receptor can also cause pain and itch and, it may not be coincidental that orgasm in some individuals can be enhanced by pain. “It is well known that neurogenic inflammation is associated with the activation of nociceptors [pain receptors] sensitive to capsaicin ...” (Origoni, 2014, pg. 5).
The NIACIN FLUSH and the TRPV1 “Capsaicin” receptor—the connection to better orgasms
Durk has commented that he finds that experiencing the niacin flush while having an orgasm produces a stronger orgasm. (Sandy has noticed that, too.) Recently, niacin has been discovered to activate the TRPV1 receptor (Linlin, 2014) and this is thought by the researchers who made that discovery to be a part of the niacin flush of itching and increased cutaneous (skin) blood flow with the sensation of warmth. Incidentally, we find here the return of the inflammatory prostaglandin PGE2 and its counteractive antiinflammatory prostaglandin PGD2 in the pain activation at the irritant receptor TRPA1 (related to and interactive with TRPV1). The TRPA1 receptor is activated by pungent, warming spices, such as mustard, garlic, and cinnamon (Materazzi, 2008). As explained in Sandy Shaw’s paper on the niacin flush (see Life Enhancement website for August, September, and October 2015), the pulsatile release of PGD2 by immediate release (not extended release) niacin is the cause of the niacin flush. Niacin has been shown to activate, as part of the niacin flush, the TRPV1 receptor (as does capsaicin) (Linlin, 2014) and perhaps, like capsaicin, this activation could desensitize the TRPV1 receptors.
These anecdotal observations and very recent scientific discoveries are consistent with TRPV1 activation being part of orgasm.
It is known that, “Sexual experience promotes adult neurogenesis in the hippocampus despite an initial elevation in stress hormones,” as it says in the title of a paper by Leuner, Glasper, Gould, PLoS ONE July 2010. This is consistent with the increased neuronal excitation required for neurogenesis and, thus, neurogenesis and orgasm may be cousins in terms of electrical pathways. Now if only we could figure out how to generate orgasms at will and perhaps lengthen them (much too short, like life itself, don’t ya think?)
It may be that a simple way to increase the strength and/or length of orgasms is to activate the TRPV1 receptors at the time that you want to experience an orgasm. Hence, eating hot pepper, cinnamon, ginger, mustard, garlic, or other “hot” foods and spices just before you want to “come” might be just the ticket. In fact, “hot” foods and spices have long been thought to be aphrodisiac and the TRPV1 receptor activation may be a large part of why they appear to have sex enhancing effects. Hot Indian spices are indeed used in Tantric yoga sex ceremonies as we found when we were guinea pigs in studies of tantric sex by doctors Hartman and Fithian in the 1970s.
IN FACT, HOT FOODS AND SPICES
MAY HELP YOU LIVE LONGER
TRPV1 Regulates Longevity and Metabolic Health in Mice
Indeed, TRPV1 does a lot more than regulate pain and itch and (perhaps) orgasms. It has recently been found that TRPV1 knockout mice (mice that have no TRPV1 receptors, with the result looking as if their TRPV1 receptors are entirely desensitized) are exceptionally long-lived, “displaying a youthful metabolic profile at old age.” “These data suggest that ablation of select pain sensory receptors or the inhibition of CGRP [calcitonin gene-related peptide, which promotes neurogenic inflammation or antagonizes insulin release] are associated with increased metabolic health and control longevity” (Riera, 2014). This suggests that the niacin flush and the consumption of “hot” foods and spices may be beneficial to one’s health and longevity.
TRPA1: a Gatekeeper for Inflammation
TRPA1 has been described as a “gatekeeper of chronic inflammatory disorders of the skin, airways, and gastrointestinal tract” (Bautista, 2013).
It has been linked to diseases that include asthma, cough, inflammatory bowel disease, colitis, and many others (Bautista, 2013). Hence, consuming hot foods and spices that activate the TRPA1 receptor—including mustard, garlic, cinnamon, etc.—is a way to desensitize the TRPA1 receptor, which studies show to decrease inflammation in the skin, airways, and GI tract, and possibly to extend life and induce stronger orgasms. WOW! What more could you ask?
TRPV1 Desensitization Also Improves Cognitive Function
You might add to the list of potential benefits of TRPV1 desensitization that, “TRPV1 inactivation [via desensitization] also improves cognitive functions” (Steculorum, 2014). TRPV1 has been reported to be highly expressed in brain areas important in cognitive function including the cortex and hippocampus and to modulate hippocampal synaptic plasticity including long term potentiation (Mezey, 2000). A more recent paper reported that, in mouse brain slices, capsaicin-induced changes in long term potentiation (LTP, a learning/memory process) in the lateral amygdala were mediated by TRPV1 (Zschenderlein, 2011).
Sandy (and Durk) have both noticed a REALLY remarkable improvement in Sandy’s visuo-spatial capabilities since using TRPV1 desensitization agonists as adjunct treatments for her temporal lobe epilepsy. This is an anecdotal report, not PROOF that TRPV1 activation followed by desensitization can improve visuo-spatial capabilities. Incidentally, the downside of this improved cognition via TRPV1 was, for Sandy, a concurrent increase in irritability, as well as impatience, so if you are prone to outbursts of irritability, be careful, and if you aren’t but your best friend using these supplements is, you might also be careful. Depending on how sensitive an individual is to the TRP system, changes in dietary constituents that affect TRP channels could have a noticeable effect on personality. The effect might be considered desirable by friends, but also might be undesirable—depending on how you use the supplements.
CAUTIONARY NOTES FOR THE USE OF SUPPLEMENTS THAT ACTIVATE OR DESENSITIZE TRP CHANNELS:
TRPV1 Sensitization May Be Part of Opiate (or Sex?) Withdrawal
by Sandy Shaw
There is a scientific literature describing connection between opioids and TRPV1 receptors (Hakimizadeh, 2014). In this particular paper, it was reported that in rats, morphine reduced the expression of TRPV1 receptors in the amygdala but not in the hippocampus. The amygdala is an important brain center involved with, among other things, the emotion of fear. The researchers (Hakimizadeh, 2014) found that in morphine-dependent rats, there was a significant decrease in TRPV1 gene expression in the amygdala and that this suggests that, “TRPV1 receptors may be involved in morphine-induced dependence.”
Sex addiction might be an example of what happens when endogenous (or exogenous) opioids interact with TRPV1 receptors, but it is quite complex because, for one thing, there are 28 different known Transient Receptor Potential (TRP) channels, and these may interact with each other, with feedback effects and compensatory activity that complicates the interpretation of these interactions (Kaneko, 2014).
For those with deficient interest in sex (the so-called “hypoactive sexual desire disorder”), TRPV1 activators (capsaicin and ginger, for example) may be useful in jazzing up sexual interest. Perhaps that is a reason that ginger beer (real beer, not a soft drink) is so popular. Actually, the soft drink would work, too, but small amounts of alcohol boost the TRPV1 effect of the ginger.
COMING UP: perhaps in next Durk & Sandy newsletter:
TRPV1 And Drugs, Sex, (And Rock & Roll?)
Hmmmm. I wouldn’t be surprised if TRPV1 plays a role in rock & roll by being part of the system that, particularly in young men (but also some young women) puts the energy and the sexual drive into rock & roll that you don’t see too much in aging rock performers. Does this mean that old rock performers can be “rejuvenated” by TRPV1 agonists??? A fun thought for the future of rock & roll.
Also, as noted above (see section on TRPV1 improvement of cognition), this receptor may be involved with visuo-spatial abilities (only a hypothesis), as Sandy and Durk have noted in Sandy, who has sensitivity to TRPV1 receptors. If so, then here is another way that TRPV1 agonists might be beneficial to aging musicians.
Yummy and SO easy to make. Other than shopping for the ingredients, prep time is only about 10 minutes.
Nutritional benefits: 1. sweetened with erythritol, 2. the whipped topping is made of low fat, low sugar content chocolate mousse yogurt with live cultures. Erythritol is not only free of sucrose or sweeteners, both natural and synthetic, with various adverse effects, but it is a scavenger of damaging hydroxyl radicals. 3. Vanilla is a mild agonist to the TRPV1 receptor, while nutmeg in the quantities used for the cheesecake will give you, in a serving, a mild agonist dose to the TRPA1 receptor. Ever think of eating as a virtual chemistry book of ingredients and their effects? These days, it can seem a lot like that. Your taste buds won’t know the difference, though. It will all just taste wonderful to them.
Ingredients you’ll need:
• Canned pineapple slices in pineapple juice, six or seven slices
• 1 prepared graham cracker pie crust
• 1 pkg (8 oz) of cream cheese, softened
• Two or three 6 oz. servings of Yoplait whipped chocolate
• Mousse yogurt
• 2 teaspoons vanilla extract
• Powdered nutmeg
• 1⁄3 cup erythritol
TIP: You don’t need to bake the prepared pie crust, though the package wrapper is likely to suggest it if you want a “golden” crust. The flavor difference is not very much whether “golden” or not.
1. Use a hand mixer or whip to blend the softened cream cheese and vanilla in a small bowl.
2. Line the pie crust with the drained slices of pineapple.
3. Pour the cream cheese and vanilla mixture evenly over the pineapple slices.
4. Sprinkle nutmeg over the cream cheese/vanilla layer to your taste.
5. Gently spoon out the chocolate mousse yogurt over the cream cheese/vanilla until even, without pressing down on it (so as to avoid squeezing out the air whipped into the mousse).
6. That’s it! You cover your pie shell containing its fillings with the plastic cover that generally comes with the prepared pie crust and refrigerate for three hours. Then ENJOY!!
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